Preliminary evidence that acute stress moderates basal testosterone's association with retaliatory behavior.

A contribution to a special issue on Hormones and Human Competition. Testosterone is theorized to increase retaliation after social provocation. However, empirical evidence in support of these theories is mixed. The present research investigated whether acute stress causally suppresses testosterone's association with retaliation. We also explored sex differences in behavioral responses to acute stress. Thirty-nine participants (51.28% male) were randomly assigned to a high- or low-stress condition. Then participants engaged in 20 one-shot rounds of the ultimatum game, which was used to assess retaliatory behavioral responses to unfair treatment. Participants provided two saliva samples to measure testosterone and cortisol concentrations - one sample before the stress manipulation, and the second after the ultimatum game (20minutes post-stressor). Results revealed a positive association between basal testosterone and retaliation in the low-stress condition, but not in the high-stress condition. Further, cortisol concentrations increased in the high- compared to the low-stress condition, and these cortisol changes moderated the association between basal testosterone and retaliation. The associations between basal testosterone and retaliation under varying levels of stress were similar in men and women. However, there was a sex difference in behavioral responses to the stress manipulation that was independent of testosterone. In women, the high-stress condition reduced retaliation compared to the low-stress condition, whereas in men the opposite pattern emerged. Collectively, this study (i) provides preliminary evidence that experimentally manipulated stress blocks basal testosterone's association with retaliation, and (ii) reveals a sex difference in retaliation under varying levels of stress. Discussion focuses on mechanisms, limitations, and the need for follow-up studies with larger sample sizes.

Eosinophil cationic protein: is it useful in asthma? A systematic review.

INTRODUCTION: Eosinophil cationic protein (ECP) has been widely investigated as a potential biomarker of airway inflammation. METHOD: A systematic review was performed using Medline with key terms eosinophil cationic protein and asthma, limiting the search to titles or abstracts. Out of 688 potential papers found, abstracts were reviewed based on the following criteria: (1) ECP was used as a biological marker, (2) asthma was the index disease studied, (3) it was a controlled clinical study and (4) ECP was assessed as a diagnostic, assessment or management tool. One hundred and sixty-nine articles satisfied the selection criteria and their full-text versions were reviewed. Only 53 papers were found to provide clinically useful information. RESULTS: ECP has been measured in serum, plasma, sputum, saliva and broncho-alveolar lavage fluids but serum and sputum are the most established. Levels of ECP in normal and asthmatic subjects in various body fluids were identified. ECP correlates well with airway inflammation but not airway hyper-responsiveness. It is raised in other atopic diseases and hence is not diagnostic for asthma. However, it has been shown to be useful in assessing asthma severity, compliance with anti-inflammatory asthma therapy and as a guide to tailing down inhaled corticosteroid therapy. Although there is some evidence that ECP levels are affected by age, smoking, circadian rhythm and seasonal variation, only smoking appears to be of clinical significance. DISCUSSION: Despite its limitations, ECP remains potentially useful in asthma management. Future research on ECP should focus on using serial measurements and combining it with other markers of asthma which may increase its clinical usefulness.